The purpose of this project is to fully evaluate the effect of hemorrhagic shock on neutrophil function. Initial goals of the grant are to determine the role of severe hemorrhagic shock on chemotaxis, phagocytosis and bactericidal activity. The presence of circulating inhibitors of neutrophil function as well as activated complement components will be tested from baboons' sera. It is intended to correlate PMN dysfunction with other components of cellular dysfunction which will be measured concomitantly. As has been noted in the Research Plan, liver and muscle cell transmembrane potential changes will be studied throughout the duraction of the shock state. Blood gases, base deficit and serum electrolytes will also be monitored in order to determine what factors are involved in this cellular dysfunction. It has been noted that neutrophil degranulation is thought to be a major mechanism of cellular deactivation both in vitro and in vivo. Whether the neutrophil is similarly effected in hemorrhagic shock is not yet known. However, to determine if such a phenomenon occurs in the cells of shock animals, enzyme levels of cells and enzyme levels in the serum will be studied. Finally, the role of membrane receptor availability in normal and shocked baboons will be studied to determine the availability of receptors in PMN dysfunction. It is hoped that a better understanding of the mechanism causing impaired neutrophil responsiveness in shock will lead to a more rational approach to future therapy.